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Thermoregulatory Vasoconstriction During Propofol/Nitrous Oxide Anesthesia in Humans

Threshold and Oxyhemoglobin Saturation

Department of Anesthesia, University of California, San Francisco, California; Department of Anesthesiology, University of Minnesota, Minneapolis; and the Department of Surgery, University of Melborne, Victoria, Australia

Abstract

To determine the thermoregulatory effects of propofol and nitrous oxide, we measured the threshold for peripheral vasoconstriction in seven volunteers over a total of 13 study days. We also evaluated the effect of vasoconstriction on oxyhemoglobin saturation (Spo₂). Anesthesia was induced with an intravenous bolus dose of propofol (2 mg/kg), followed by an infusion of 180 µg.kg^–1.min^–1 for 15 min, and maintained with 60% nitrous oxide and propofol (80–160 µg.kg^–1.min^–1). Central and skin surface temperatures and Spo₂ (using two different pulse oximeters) were measured continuously; plasma propofol concentrations and arterial Po₂ were measured at 15-min intervals. Volunteers were cooled with a circulating water blanket until definitive peripheral vasoconstriction was detected. The tympanic membrane temperature triggering vasoconstriction was considered the thermoregulatory threshold. Vasoconstriction developed on seven study days during propofol/nitrous oxide anesthesia at a central temperature of 33.3 ± 1.0°C (mean ± SD) and plasma propofol concentration of 3.9 ± 1.1 µg/mL. The thresholds during anesthesia were significantly lower than those during the control period (36.7 ± 0.3°C), but the correlation between plasma propofol concentrations and vasoconstriction thresholds was poor. On the remaining six study days, vasoconstriction did not develop despite central temperatures ranging from 32.1 to 32.7°C. Corresponding propofol concentrations were 4.1–10.9 µg/mL. These data suggest that anesthesia with propofol, in typical clinical concentrations, and 60% nitrous oxide substantially inhibits thermoregulatory vasoconstriction. Vasoconstriction increased Spo₂by approximately 2% without a significant concomitant change in Po₂. The observed increase in Spo₂ probably reflects decreased transmission of arterial pulsations to venous blood in the finger.

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